The structural and functional relationship in the mechanism by which glycoprotein hormones (thyrotropin), certain bacterial toxins (cholera and pertussis, for example), the antiviral protective agent, interferon, Alpha-1 adrenergic agents, insulin, and insulin-like growth factors (I and II), interact with and transmit their message through the cell membrane to affect thyroid function and pathology, is being further defined. Studies using monoclonal antibodies and the idiotype-antiidiotype theory have continued to explore the importance of these relationships to the expression of thyroid hyperfunction in Graves' disease; to organ-specific autoimmunity in general and the autoimmunity of Graves' disease in particular; to fluid losses in intestinal diarrhetic states; to thyroid storm and the sympathetic overactivity syndrome of tetanus; to the ability of hormones to modulate the oncogenic state; and to the mechanism by which toxins subvert normal mechanisms to impose their pathological effects. Studies have been continued which evaluate the role of membranes in thyroglobulin biosynthesis and thyroglobulin biodegradation to T3 and T4 and role of carbohydrate moieties in thyroglobulin structure and post-translation processing. Studies also continue to explore lipid regulation of receptor expression with special emphasis on neuronal and thyroid cell growth and development.